initially respond eventually relapse because their cancer has
become resistant to crizotinib ( 95).

NSCLC resistance to crizotinib occurs through a varietyof molecular mechanisms, including the emergence ofnew mutations in ALK ( 96) (see sidebar on The Challengeof Treatment Resistance). Recent research has shown thatceritinib is able to block many of the unique forms ofALK that result from these new mutations ( 97). In thisway, ceritinib benefits many patients, like James (Rocky)Lagno (see p. 62), with crizotinib-resistant NSCLC drivenby ALK ( 98).